Atrial Fibrillation (AF) is the most common cardiac arrhythmia that requires treatment and involves the two upper chambers (atria) of the heart. Approximately 2.2 million individuals in the United States and 4.5 million in the European Union have AF (Camm et al. 2010. Eur Heart J. 31:2369-2429; Go et al. 2001. JAMA 285:2370-2375). It also accounts for ⅓ of hospital admissions for cardiac rhythm disturbances (Fuster et al. 2006. Circulation 114:e257-354), and the rate of admissions for AF has risen in recent years (Fri berg et al. 2004. Epidemiology 14: 666-672). The prevalence of AF increases with age, from 0.5% at 40-50 years, to 5-15% at 80 years (Camm et al. 2010. Eur Heart J. 31:2369-2429). The incidence of atrial fibrillation also increases with age. In developed countries, the number of patients with atrial fibrillation is likely to increase during the next 50 years, due to the growing proportion of elderly individuals (Go et al. 2001. JAMA 285: 2370-2375).
Its name comes from the fibrillating (i.e., quivering) of the heart muscles of the atria, instead of a coordinated contraction. It can often be identified by taking a pulse and observing that the heartbeats do not occur at regular intervals. However, a stronger indicator of AF is the absence of P waves on an electrocardiogram (ECG or EKG), which are normally present when there is a coordinated atrial contraction at the beginning of each heart beat.
AF is associated with altered tolerance and increased risk of death, independently of other cardiac risk factors (Benjamin et al. 1998. Circulation 98: 946-952). The most prevalent and devastating consequence of AF is stroke. Strokes from AF account for 6-24% of all ischemic strokes (Narumiya et al. 2003. Circulation Journal 67 (1): 68-72). Electrical and pharmacological cardioversion of AF may be complicated of stroke following the restoration of an atrial mechanical activity (Camm et al. 2010. Eur Heart J. 31:2369-2429; Halperin et al. 1988. Stroke 19:937-941).
The American College of Cardiology (ACC), American Heart Association (AHA), and the European Society of Cardiology (ESC) recommend in their guidelines the following classification system based on simplicity and clinical relevance (Fuster et al. 2006. Circulation 114:e257-354). All atrial fibrillation patients are initially in the category called first detected AF. These patients may or may not have had previous undetected episodes. If a first detected episode self-terminates in less than 7 days and then another episode begins later on, the case has moved into the category of paroxysmal AF. Although patients in this category have episodes lasting up to 7 days, in most cases of paroxysmal AF the episodes will self-terminate in less than 24 hours. If instead the episode lasts for more than 7 days, it is unlikely to self-terminate (Levy 2000. Curr Opin Cardiol 15: 54-57) and it is called persistent AF. In this case, the episode may be terminated by cardioversion. If cardioversion is unsuccessful or it is not attempted, and the episode is ongoing for a long time (e.g. a year or more), the patient's AF is called permanent.
In addition to the above four AF categories, which are mainly defined by episode timing and termination, the ACC/AHA/ESC guidelines describe additional AF categories in terms of other characteristics of the patient (Fuster et al. 2006. Circulation 114:e257-354): Lone atrial fibrillation (LAF)—absence of clinical or echocardiographic findings of other cardiovascular disease (including hypertension), related pulmonary disease, or cardiac abnormalities such as enlargement of the left atrium, and age under 60 years; Nonvalvular AF—absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair; Secondary AF—occurs in the setting of a primary condition which may be the cause of the AF, such as acute myocardial infarction, cardiac surgery, pericarditis, myocarditis, hyperthyroidism, pulmonary embolism, pneumonia, or other acute pulmonary disease.
Atrial fibrillation is usually accompanied by symptoms related to a rapid heart rate. Rapid and irregular heart rates may be perceived as palpitations, exercise intolerance, and occasionally produce angina (if the rate is faster and puts the heart under strain) and congestive symptoms of shortness of breath or edema. Sometimes the arrhythmia will be identified only with the onset of a stroke or a transient ischemic attack (TIA). It is not uncommon for a patient to first become aware of AF from a routine physical examination or ECG, as it may be asymptomatic in many cases (Fuster et al. 2006. Circulation 114:e257-354).
As most cases of atrial fibrillation are secondary to other medical problems, the presence of chest pain or angina, symptoms of hyperthyroidism (an overactive thyroid gland) such as weight loss and diarrhea, and symptoms suggestive of lung disease would indicate an underlying cause. A previous history of stroke or TIA, as well as hypertension (high blood pressure), diabetes, heart failure and rheumatic fever, may indicate whether someone with AF is at a higher risk of complications (Fuster et al. 2006. Circulation 114:e257-354).
Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Cardioversion is a noninvasive conversion of an irregular heartbeat to a normal heartbeat using electrical or chemical means (Fuster et al. 2006. Circulation 114:e257-354). Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as aspirin, heparin, warfarin or dabigatran to protect them from stroke.
The duration of AF becomes important when cardioversion is being considered, and it is generally accepted that patients who have an episode of AF of less than 48 hours may undergo prompt cardioversion safely whereas patients with an AF>48 hours have to be treated with anticoagulants for more than 3 weeks or to undergo transesophageal echocardiogram (TEE) prior to cardioversion (Camm et al. 2010. Eur Heart J. 31:2369-2429; Fuster et al. 2006. Circulation 114:e257-354; Page et al. 2004. NEJM 351:2408-2416; Klein et al. 2001. NEJM 344:1411-1420; Jessup et al. 2009. Circulation 119:1977-2016). The duration of AF may be determined in patients who report acute palpitations, dyspnoea or syncope. However, asymptomatic or silent AF occurs frequently (Savelieva et al. 2000. Pacing din Electrophysiol 23:145-148): in the Canadian registry of AF, 21% of patients with newly diagnosed AF were asymptomatic (Kerr et al., 1996. Eur Heart J 17 Suppl C:48-51). In another study, 17% of patients had asymptomatic episodes of AF before they noted AF-related symptoms (Page et al. 2003. Circulation 107:1141-5). Overall, the clinical determination of the duration of AF, below or above 48 h, might be often hazardous in clinical practice pointing out the need for new tools to help clinicians in the accurate determination of AF duration prior to presentation.
Previous studies have suggested the possible merit of some biomarkers, mainly B-type natriuretic peptides, in the risk stratification of patients with AF or the prediction of AF occurrence (Defteros et at 2010. Heart 96:1033-1036; Jourdain et al. 2002. Eur J Heart Fail 4:263-267; Maisel et al. 2002. NOM 347:161-167; Thejus et al. 2009. Indian Pacing Electrophysiol J 9:1-4). Deftereos and collegues reported that patients with AF of less than 24 h and no heart failure have a particular pattern of NT-proBNP fluctuations that is characterized by a progressive rise within the first 24 h followed by rapid decline (Defteros et al. 2010. Heart 96:1033-1036). They concluded that obtaining two to three plasma NT-proBNP levels within 24 hours of presentation in patients with AF without heart failure, who cannot satisfactorily pinpoint the time of onset, may assist in determining whether the onset of the arrhythmia was recent, and that such information would be pertinent to decisions concerning anticoagulation and cardioversion. However, the triage of patients based on such NT-proBNP fluctuations may be hazardous in clinical practice and need prolonged monitoring of patients before a decision can be reached. In contrast, Tsuchida and Tanabe demonstrated that BNP was already elevated immediately within 4 hours after onset of AF and that the BNP level was not significantly correlated with the time elapsed after AF onset (Tsuchida and Tanabe 2004. J Cardiol 44:1-11).